Affinity pump system: a new peristaltic blood pump for cardiopulmonary bypass

An in vitro study has been carried out to assess the pump performance of a new peristaltic, extracorporeal displacement pump (Affinity) for cardiopulmonary bypass. The pump system consists of a pump rotor (0-110 rpm), a pump chamber, a venous reservoir with a 5/8" connecting tube and the Affinity console. The polyurethane chamber is connected to the venous reservoir by a 5/8" tube and fills passively due to the hydrostatic pressure exhibited by the fluid height in the venous reservoir. The implementation of an occlusive segment in the pump chamber, which collapses in low filling states, should prevent significant negative pressures. An in vitro circuit was filled with bovine blood (37 degrees C, hematocrit 35%) and the pump flow was measured by an ultrasonic transit time flow probe with respect to pre-load, diameter and length of attached tubing in the venous line, pump speed (rpm) and size of the connecting tube (3/8" and 5/8"). At 108 rpm and a preload equal to 10 mmHg, the flow was 8.6 +/- 0.42 l/min for an afterload of 80 mmHg. The reduction of the inlet connector to 3/8" diminished the pump flow significantly to 5.2 +/- 0.31 l/min (p < 0.0001). The pump flow decreased linearly with respect to the length of the attached tube in the venous line and for a 2 m long 5/8" silicon tube, the rpm-optimized flow was still 6.0 +/- 0.28 l/min at a preload of 10 mmHg. In case of low filling state or too high rpm, the occlusive segment collapsed and no cavitation bubbles could be detected. Our in vitro measurements yield a nomogram for rpm-optimized blood flow with respect to the pre-load in the venous reservoir. The delivered 5/8"connecting tube facilitates optimum filling of the pump chamber for high blood flow, but limits the use of venous reservoirs to Affinity products. The pump yields a high blood flow even when long tubing in the venous line is used. This makes the pump a candidate for a ventricular assist device. In hypovolemia or high rpm, the occlusive segment collapses and no negative pressure is generated at the inflow site of the pump chamber.     

Effects of alterations in left ventricular filling, contractility, and systemic vascular resistance on the ascending aortic blood velocity waveform of normal subjects.

OBJECTIVES: To confirm the consistent effects on Doppler-measured aortic blood flow velocity waveform variables of alterations in left ventricular preload, afterload, and inotropy using pharmacologic and physiologic maneuvers. SETTING: Medical school laboratory. SUBJECTS: Healthy volunteers. INTERVENTIONS: Increasing infusion rates of dobutamine (1.25 to 5 micrograms/kg.min), esmolol (1.25 to 5 mg/min), phentolamine (1.25 to 5 mg/min), methoxamine (1.25 to 5 mg/min), metaraminol (1.25 to 5 mg/min), and placebo (1.25 to 5 mL of 0.9% saline/min) and increasing plasma removal (0.5 to 1 L) in awake, rested, supine subjects. MEASUREMENTS AND MAIN RESULTS: Ascending aortic blood flow was measured by the suprasternal Doppler approach allowing calculation of waveform variables of stroke distance and minute distance (linear measures of stroke volume and cardiac output), peak velocity, mean acceleration and flow time corrected for heart rate. An index of systemic vascular resistance was obtained by dividing mean systemic BP by the minute distance. Inotropic changes predominantly affected peak velocity and mean acceleration. Changes in preload mainly affected the flow time corrected for heart rate, whereas afterload changes had an intermediate effect. Unsuspected but subsequently confirmed hemodynamic effects were seen with esmolol and metaraminol. CONCLUSIONS: Aortic blood flow velocity waveform variables measured by Doppler ultrasound can be used to noninvasively follow changes in left ventricular preload, afterload, and inotropy.     

Left ventricular end-diastolic pressure can be estimated by either changes in transmitral inflow pattern during valsalva maneuver or analysis of pulmonary venous flow.

We directly compared the transmitral inflow pattern during preload reduction and pulmonary venous flow velocities to determine left ventricular end-diastolic pressure (LVEDP) in 78 patients who underwent left heart catheterization. Transmitral inflow indexes (A-wave duration, ratio of peak flow velocity of early diastole [E] to peak flow velocity of late diastole during atrial contraction [A] [E/A ratio]) at rest and during the Valsalva maneuver (30 mm Hg for 15 seconds) and indexes of pulmonary venous flow (velocity and duration of the atrial reversal) were obtained. Fair correlations existed between LVEDP (mean 15+/-6 mm Hg) and the percentage decrease in the E/A ratio (r = 0.72), increase in duration of A wave during the Valsalva maneuver (r = 0.60), flow velocity of atrial reversal (r = 0.58), and difference of duration of atrial flow reversal and A wave (r = 0.62) (all P<.001). While sensitivity, specificity, and diagnostic accuracy to detect an elevated LVEDP were comparable, technically adequate Doppler recordings were obtained more often for the mitral inflow during the Valsalva maneuver than for the pulmonary venous flow (72 versus 66 patients, P< 0.05).     

Acute alterations of pre- and afterload: Are Doppler-derived diastolic filling patterns able to differentiate the loading condition?

The net effects of acute changes in pre- and afterload on left ventricular filling, were examined by altering loading conditions in normal subjects. The specific purpose of this study was to investigate whether Dopplerderived transmitral flow patterns are able to differentiate the type of loading conditions. In 24 normal subjects (13 females, 11 males, mean age 44.1±11.5 years), the following Doppler variables were determined at baseline, after rapid volume infusion (preload increase), after nitroglycerin administration (preload decrease), during isometric exercise (afterload increase), and after application of a converting enzyme inhibitor (afterload decrease): the peak and integrated early (E, Ei) and late (A, Ai) diastolic flow velocities, their ratios (E/A, Ei/Ai), the percentage of atrial contribution (ACON), and the acceleration and deceleration times (Ac, dc) of early filling. Reduced preload and increased afterload led to similar filling patterns characterized by a significant E and Ei decrease (p<0.05, compared to baseline) accompanied by an A and Ai increase with a resultant reduction of E/A and Ei/Ai. Both changes increased the atrial contribution to filling and reduced Ac and dc. Increased preload only significantly increased E and Ei, while reduced afterload did not induce any significant changes. Different loading conditions alter Doppler-derived diastolic filling patterns. However, the transmitral flow profile is not specific enough to distinguish the manner in which loading conditions have been altered.     

Decline of atrial natriuretic peptide release in dogs during sustained rapid cardiac pacing

1. To assess the ability of the atria to maintain elevated plasma concentrations of atrial natriuretic peptide (ANP), the temporal changes in plasma ANP concentrations were studied in seven chloralose-anaesthetized dogs during 4 h of sustained rapid cardiac pacing. 2. Heart rate increased from 124 +/- 26 (mean +/- SEM) to 278 +/- 28 beats/min for the 4 h duration of rapid cardiac pacing. Mean pulmonary wedge pressure increased from 3.6 +/- 1.8 to 17.4 +/- 7.1 mmHg at 30 min (P less than 0.01) and mean right atrial pressure rose from -1.7 +/- 1.9 to 2.0 +/- 2.8 mmHg at 30 min (P less than 0.01). Both remained constant at these elevated pressures for the entire 240 min of rapid pacing. 3. Arterial ANP concentrations increased in all dogs from 87 +/- 11 to a maximum of 1263 +/- 592 pmol/l at 30 min (P less than 0.01), falling to 411 +/- 42 pmol/l after 60 min and to 146 +/- 70 pmol/l after 240 min of rapid continuous pacing (P less than 0.01 compared with 30 min). Coronary sinus ANP concentrations showed a similar pattern, rising from 241 +/- 79 to a maximum of 1837 +/- 203 pmol/l after 30 min (P less than 0.01). These peak values likewise were not sustained, falling to 962 +/- 198 pmol/l after 60 min and 297 +/- 41 pmol/l after 240 min of rapid pacing (P less than 0.01 compared with 30 min). 4. It is concluded that atria are unable to maintain the peak concentrations of ANP reached after 30 min of rapid pacing despite persistently elevated atrial pressures.     

Effects of volume loading on left atrial systolic time intervals.

The effects of volume loading on the left atrial preejection period (LAPEP) and left atrial ejection time (LAET) were examined in 24 patients with various heart diseases using pulsed Doppler echocardiography. In response to volume loading, the left atrial dimension before atrial contraction significantly increased from 30.6 mm +/- 5.8 mm to 32.4 mm +/- 5.4 mm and the change in the left atrial dimension during atrial contraction tended to increase. The peak velocity in the atrial contraction phase significantly increased from 58 cm/s +/- 14 cm/s to 63 cm/s +/- 13 cm/s, and the integral of the atrial contraction phase tended to increase. LAPEP significantly decreased from 114 ms +/- 16 ms to 104 ms +/- 14 ms and LAET significantly decreased from 128 ms +/- 15 ms to 124 +/- 12 ms. The relation between LAET and left ventricular end-diastolic pressure, and that between LAPEP and mean pulmonary capillary wedge pressure, shifted downward to the right after volume loading. Thus, left atrial ejection is augmented by volume loading according to the Frank-Starling mechanism, while LAPEP decreases due to an increase in preload and LAET decreases due to an increase in afterload.     

Doppler characteristics of late-diastolic flow in the left ventricular outflow tract

This study characterizes the relationship between late-diastolic Doppler detected forward flow in the left ventricular outflow tract and diastolic transmitral flow. Pulsed-wave Doppler interrogation of the left ventricular outflow tract, in a prospective consecutive series (n = 137), revealed the presence of end-diastolic forward flow in 83% of the patients studied. Further quantification of both flow signals was performed in 67 patients. Pulsed-wave mapping demonstrated that peak velocity of the end-diastolic left ventricular outflow tract signal (J wave) was maximal, 2.6 +/- 0.7 cm from the aortic valve anulus, and occurred 48 +/- 34 milliseconds after the peak transmitral atrial velocity flow signal. Peak J velocity ranged from 25 to 118 cm per second and correlated with peak A velocity (r = 0.69, p less than 0.001). Peak J velocity was inversely related to left ventricular end-diastolic dimension (r = -0.53, p less than 0.0001) and left ventricular end-diastolic volume (r = -0.43, p less than 0.004). There was no relationship between J wave velocity and early diastolic filling. We concluded that a late-diastolic forward flow signal is commonly observed in the left ventricular outflow tract. It is a manifestation of transmitral atrial systolic flow in the left ventricular outflow tract and is determined predominantly by peak transmitral atrial velocity and left ventricular size.     

The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man.

Sequential determinations of glucose outflow and inflow, and rates of gluconeogenesis from alanine, before, during and after insulin-induced hypoglycemia were obtained in relation to alterations in circulating epinephrine, norepinephrine, glucagon, cortisol, and growth hormone in six normal subjects. Insulin decreased the mean (+/-SEM) plasma glucose from 89+/-3 to 39+/-2 mg/dl 25 min after injection, but this decline ceased despite serum insulin levels of 153+/-22 mul/ml. Before insulin, glucose inflow and outflow were constant averaging 125.3+/-7.1 mg/kg per h. 15 min after insulin, mean glucose outflow increased threefold, but then decreased at 25 min, reaching a rate 15% less than the preinsulin rate. Glucose inflow decreased 80% 15 min after insulin, but increased at 25 min, reaching a maximum of twice the basal rate. Gluconeogenesis from alanine decreased 68% 15 min after insulin, but returned to preinsulin rates at 25 min, and remained constant for the next 25 min, after which it increased linearly. A fourfold increase in mean plasma epinephrine was found 20 min after insulin, with maximal levels 50 times basal. Plasma norepinephrine concentrations first increased significantly at 25 min after insulin, whereas significantly increased levels of cortisol and glucagon occurred at 30 min, and growth hormone at 40 min after insulin. Thus, insulin-induced hypoglycemia in man results from both a decrease in glucose production and an increase in glucose utilization. Accelerated glycogenolysis produced much of the initial, posthypoglycemic increment in glucose production. The contribution of glycogenolysis decreased with time, while that of gluconeogenesis from alanine increased. Of the hormones studied, only the increments in plasma catecholamines preceded or coincided with the measured increase in glucose production after hypoglycemia. It therefore seems probable that adrenergic mechanisms play a major role in the initiation of counter-regulatory responses to insulin-induced hypoglycemia in man.     

Endothelin-1-induced renal vasoconstriction is blunted by enalaprilat and enhanced by EDRF antagonist in awake normotensive rats.

We attempt to elucidate the putative indirect mechanisms by which endothelin-1 affects mean blood pressure and renal blood flow in normotensive awake rats. Endothelin-1 (700 pg/kg, i.v.) induced a short-lasting decrease followed by a prolonged increase in mean blood pressure (from 113 +/- 4 to 92 +/- 4 mmHg at 30 sec, 132 +/- 7 mmHg at 10 min, and 129 +/- 6 mmHg at 30 min, p less than 0.01), and caused a profound and long-lasting fall in renal blood flow as measured by Doppler flowmeter technique (from 2.87 +/- 0.29 to 1.40 +/- 0.37 kHz at 30 sec, 1.77 +/- 0.32 kHz at 10 min and 2.10 +/- 0.45 kHz at 30 min, p less than 0.01). Neither the receptor antagonist of bradykinin D-Arg0-Hyp3-Thi5,8-DPhe7-bradykinin (30 micrograms/kg/min, i.v.) nor the antagonist of angiotensin II Sar1, Thr8-angiotensin II (4 micrograms/kg/min, i.v.) altered the changes in mean blood pressure and renal blood flow induced by endothelin-1. The antagonist of EDRF synthesis, NG-monomethyl-L-arginine (100 micrograms/kg/min, i.v.) enhanced the endothelin-1-induced increase in mean blood pressure (endothelin-1: 20 +/- 2 mmHg vs endothelin-1 + EDRF antagonist: 39 +/- 3 mmHg at 10 min, p less than 0.01) and decrease in renal blodo flow (endothelin-1: -40 +/- 4% vs endothelin-1 + EDRF antagonist: -73 +/- 3% at 10 min, p less than 0.01).2+ mediated by the blockade of angiotensin II formation.     

Duplex Doppler sonography of changes in portal vein flow in healthy term newborn infants after feeding.

To establish reference values for changes in portal venous diameter, angle- corrected maximal flow velocity, and flow in healthy term newborn infants after formula feeding, we studied 20 subjects using duplex Doppler sonography. After feeding, portal venous diameter increased from 3.6 +/- 0.1 (mean +/- standard error of the mean) to 3.9 +/- 0.1 mm at 15 min and decreased to 3.8 +/- 0.1 at 60 min. Maximal flow velocity increased from 24.1 +/- 1.3 cm/s to a maximum of 35.9 +/- 2.4 cm/s at 15 min and decreased to 28.8 +/- 1.5 cm/s at 60 min. Flow increased from 85.0 +/- 7.5 ml/min to a maximum of 153.6 +/- 14.9 ml/min at 15 min with decrease similar to the maximal flow velocity curve. We conclude that formula feeding produces peak portal blood flows of nearly twice the fasting values at 15 min after feeding and returns almost to fasting value by 60 min.     

Enalaprilat improves systemic and mesenteric blood flow during resuscitation from hemorrhagic shock in dogs

We investigated the systemic and mesenteric cardiovascular effects of administering enalaprilat during resuscitation from hemorrhage. Dogs were hemorrhaged (mean arterial pressure [MAP] 40-45 mmHg for 30 min, then 30-35 mmHg for 30 min) and were then resuscitated with intermittent lactated Ringer's solution (200 mL/kg/h during first 40 min, and 60 mL/kg/h during the following 130 min, MAP 75-80 mmHg). A constant-rate infusion of saline with or without enalaprilat (0.02 mg/kg/h) was initiated after 40 min of resuscitation. Blood flows declined with hemorrhage, increased with resuscitation, and then declined during the initial 40 min of resuscitation. Enalaprilat administration resulted in blood flow increases not seen in the controls (ending values for cardiac index: 2.8 +/- 0.4 L/min/m2 vs. 1.6 +/- 0.3 L/min/m2; celiac arterial flow 314 +/- 66 L/min/m2 vs. 139 +/- 13 mL/min/m2; and portal venous flow 596 +/- 172 L/min/m2 vs. 414 +/- 81 mL/min/m2 for enalaprilat versus controls, respectively). The greater flows with enalaprilat appeared to be due to prevention of the increases in afterload noted in the controls (ending arterial elastance values 3.73 +/- 0.97 mmHg/m2/mL vs. 7.74 +/- 1.80 mmHg/m2/mL for enalaprilat versus controls, respectively). We conclude that administration of a constant-rate infusion of enalaprilat during resuscitation can be used to improve systemic and mesenteric blood flow.     

The effects of atrial fibrillation on coronary blood flow and performance of ischaemic myocardium in dogs with coronary artery stenosis

1. Atrial fibrillation may impair coronary blood flow by tachycardia and reflex vasoconstriction. It has not been documented, however, whether in the presence of coronary stenosis atrial fibrillation exceeds the effects of rhythmic atrial tachycardia. 2. The effects of experimentally induced atrial fibrillation compared with atrial tachycardia, therefore, were tested in 22 anaesthetized dogs. Stenosis of the left anterior descending coronary artery was induced to reduce coronary blood flow by about 40%. 3. In the presence of coronary stenosis, atrial fibrillation (ventricular rate: 234 +/- 21 beats/min) reduced coronary blood flow from 58 +/- 7 to 44 +/- 8 ml min-1 100 g-1 (P less than 0.001, mean +/- SEM) and subendocardial segment shortening (ultrasonic crystals) from 12 +/- 2 to 4 +/- 2% (P less than 0.0025), and resulted in a lactate production of 30 +/- 11% (P less than 0.005 vs sinus rhythm). 4. Atrial tachycardia (heart rate: 216 +/- 21 beats/min, NS vs atrial fibrillation) did not significantly change coronary blood flow and reduced segment shortening to 7 +/- 3% (P less than 0.05 vs atrial fibrillation). Significant lactate production did not occur. 5. Since mean arterial pressure fell from 100 +/- 4 mmHg at sinus rhythm to 89 +/- 3 mmHg (P less than 0.01) during atrial fibrillation but not during atrial tachycardia, it was held constant in 13 dogs by a pressurized blood reservoir. Coronary blood flow, however, fell from 43 +/- 6 to 36 +/- 5 ml min-1 100 g-1 (P less than 0.0025). 6. Thus atrial fibrillation may reduce coronary blood flow and induce myocardial ischaemia in the presence of coronary stenosis in excess of atrial tachycardia.     

Effect of isometric exercise and autonomic blockade on the haemodynamics: a noninvasive study in healthy volunteers

Sixteen healthy young volunteers were studied with echocardiography and systolic time intervals at rest and after three minutes' isometric exercise before and during autonomic blockade with atropine and propranolol. Isometric exercise increased cardiac output by raising the heart rate from 64 +/- 3 to 72 +/- 4 bpm (SEM) (p less than 0.01). Mean blood pressure increased from 86 +/- 2 to 104 +/- 3 mmHg (p less than 0.001) without any changes in the calculated total peripheral vascular resistance. Afterload (left ventricular systolic wall stress) rose but preload (left ventricular end-diastolic diameter, LVEDD) did not change. There was no variation in fractional shortening, maximal velocity of circumfertial fibre shortening (VCFmax) or pre-ejection period (PEP) despite increased afterload. This indicates stimulated intropy during isometric exercise. Autonomic blockade enhanced cardiac output by increasing heart rate from 64 +/- 3 to 97 +/- 2 bpm (p less than 0.001). Mean blood pressure rose from 86 +/- 2 to 93 +/- 2 mmHg (p less than 0.01) while vascular resistance fell. Afterload did not change but LVEDD shortened form 45.5 +/- 0.9 to 43.5 +/- 0.9 mm (p less than 0.001). Preload-independent VCFmax did not increase despite raised heart rate. PEP rose from 99 +/- 4 to 107 +/- 3 ms (p less than 0.01) and fractional shortening fell from 29 +/- 1 to 25 +/- 1% (p less than 0.001); these changes were greater than expected from the reduced preload. Consequently autonomic blockade seems to impair myocardial contractility despite vagal dominance at rest. Heart rate and cardiac output were not influenced by isometric exercise during autonomic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of arterial and venous volume infusion on coronary perfusion pressures during canine CPR.

Intraarterial (IA) volume infusion has been reported to be more effective than intravenous (IV) infusion in treating cardiac arrest due to exsanguination. A rapid IA infusion was felt to raise intraaortic pressure and improve coronary perfusion pressure (CPP). The purpose of this study was to determine if IA or IV volume infusion could augment the effect of epinephrine on CPP during CPR in the canine model. Nineteen mongrel dogs with a mean weight of 26.3 +/- 4.2 kg were anesthetized and mechanically ventilated. Thoracic aortic (Ao), right atrial (RA) and pulmonary artery catheters were placed for hemodynamic monitoring. Additional Ao and central venous catheters were placed for volume infusion. Ventricular fibrillation was induced and Thumper CPR was begun after 5 min (t = 5). At t = 10, all dogs received 45 micrograms/kg IV epinephrine. Six animals received epinephrine alone (EPI). Five dogs received EPI plus a 500 cc bolus of normal saline over 3 min intravenously (EPI/IV). Another group (n = 8) received EPI plus the same fluid bolus through the aortic catheter (EPI/IA). Resuscitation was attempted at t = 18 using a standard protocol. There was a significant increase in CPP over baseline in all groups. The changes in CPP from baseline induced by EPI, EPI/IV and EPI/IA were 20.6 +/- 3.7, 22.8 +/- 4.2 and 22.2 +/- 2.4 mmHg, respectively. Volume loading did not augment the effect of therapeutic EPI dosing. By increasing both preload and afterload, volume administration may in fact be detrimental during CPR.     

Pediatric cardiac output measurement using surface integration of velocity vectors: an in vivo validation study

OBJECTIVE: To test the accuracy and reproducibility of systemic cardiac output (CO) measurements using surface integration of velocity vectors (SIVV) in a pediatric animal model with hemodynamic instability and to compare SIVV with traditional pulsed-wave Doppler measurements. DESIGN: Prospective, comparative study. SETTING: Animal research laboratory at a university medical center. SUBJECTS: Eight piglets weighing 10-15 kg. INTERVENTIONS: Hemodynamic instability was induced by using inhalation of isoflurane and infusions of colloid and dobutamine. MEASUREMENTS: SIVV CO was measured at the left ventricular outflow tract, the aortic valve, and ascending aorta. Transit time CO was used as the reference standard. RESULTS: There was good agreement between SIVV and transit time CO. At high frame rates, the mean difference +/- 2 SD between the two methods was 0.01+/-0.27 L/min for measurements at the left ventricular outflow tract, 0.08+/-0.26 L/min for the ascending aorta, and 0.06+/-0.25 L/min for the aortic valve. At low frame rates, measurements were 0.06+/-0.25, 0.19+/-0.32, and 0.14+/-0.30 L/min for the left ventricular outflow tract, ascending aorta, and aortic valve, respectively. There were no differences between the three sites at high frame rates. Agreement between pulsed-wave Doppler and transit time CO was poorer, with a mean difference +/- 2 SD of 0.09+/-0.93 L/min. Repeated SIVV measurements taken at a period of relative hemodynamic stability differed by a mean difference +/-2 SD of 0.01+/-0.22 L/min, with a coefficient of variation = 7.6%. Intraobserver coefficients of variation were 5.7%, 4.9%, and 4.1% at the left ventricular outflow tract, ascending aorta, and aortic valve, respectively. Interobserver variability was also small, with a coefficient of variation = 8.5%. CONCLUSIONS: SIVV is an accurate and reproducible flow measurement technique. It is a considerable improvement over currently used methods and is applicable to pediatric critical care.     

经食管超声多普勒观察肺静脉及二尖瓣血流估测肺毛细血管楔嵌压的新方法

目的：本文探讨应用多普勒超声联系观察肺静脉血流（PVF）和二尖瓣前向性血流（MIF）估测平均肺毛细血管楔嵌压（MPCWP）的新途径。方法：研究了20例正常人和28例先天性心脏病患者PVF和MIF的特征,并将其多普勒参数及两者结合衍生的指标与经导管检查测得的MPCWP进行相关比较分析。结果：患者房缩期PVF的流速时间积分与周期MIF的流速时间积分之比（Zi/Ai)与MPCWP相关性最佳（MPCWP＝－7．88＋24．13xZi/Ai,SEE=3.24mm Hg,r=0.86,P＜0.01),且多元逐步回归表明：SBP、DBP、HR、age均不影响之。以Zi/Ai＞1．05估测MPCWP＞18mmHg的敏感性100％、特异性93％。结论：Zi/Ai是判定患者MPCWP正常与否的较好指标,本研究提示超声联系观察PVF和MIF可以为无创估测MPCWP提供新途径。     

Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs

BACKGROUND: A new device, the intrathoracic pressure regulator (ITPR), was developed to generate continuous negative intrathoracic pressure during cardiopulmonary resuscitation (CPR) and allow for intermittent positive pressure ventilation. Use of the ITPR has been shown to increase vital organ perfusion and short-term survival rates in pigs. The purpose of this study was to investigate the hemodynamic and blood gas effects of more prolonged (15 min) use of the ITPR during CPR in a porcine model of cardiac arrest. METHODS: After 8 min of untreated ventricular fibrillation (VF), 16 female pigs were anaesthetized with propofol, intubated, and randomized prospectively to 15 min of either ITPR-CPR or standard (STD) CPR. Compressions were delivered at a rate of 100/min with a compression to ventilation ratio of 15:2. Ventilations were delivered with a resuscitator bag. Tracheal, aortic, right atrial, intracranial pressures (ICP), common carotid blood flow and respiratory variables were recorded continuously. Arterial and venous blood gases were collected at baseline, and after 5, 10, and 15 min of CPR. Coronary perfusion pressure (CPP) was calculated as diastolic aortic pressure-right atrial pressure. Cerebral perfusion pressure (CerPP) was calculated as mean arterial pressure (MAP)-intracranial pressure. Statistical analysis was performed with unpaired t-test and Friedman's Repeated Measures Analysis. RESULTS: ITPR-CPR when compared to STD-CPR resulted in a significant decrease in mean decompression phase (diastolic) tracheal pressure (-9+/-0.6 mmHg versus -3+/-0.3 mmHg, p<0.001), diastolic right atrial pressure (DRAP) (-0.1+/-0.2 mmHg versus 2.3+/-0.2 mmHg, p<0.001) and intracranial pressure (20.8+/-0.6 mmHg versus 23+/-0.5 mmHg, respectively, p=0.04) and a significant increase in total mean aortic pressure, coronary and cerebral perfusion pressures and end tidal carbon dioxide (ETCO(2)), (p<0.001). Common carotid artery blood flow was increased by an average of 70%, p<0.001. ABGs showed progressive metabolic acidosis in the ITPR-CPR group, but PaCO(2) remained stable at 34 mmHg for 15 min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO(2) values remaining <20 mmHg (p<0.001). PaO(2) was not different between groups. Following 23 min of cardiac arrest (15 min of CPR) ROSC was achieved in 5/8 ITPR-CPR animals versus 2/8 STD-CPR animals p=0.3. CONCLUSION: ITPR-CPR significantly improved hemodynamics, vital organ perfusion pressures and common carotid blood flow compared to STD-CPR in a porcine model of prolonged cardiac arrest and basic life support. The beneficial hemodynamic effects of ITPR-CPR were sustained at least 15 min without any compromise in oxygenation.     

Lower body positive pressure by anti-G garment inflation: a suitable method to increase pulmonary capillary wedge pressure in healthy elderly subjects

In a study on non-invasive assessment of pulmonary capillary wedge pressure (PCWP), we sought a method to increase PCWP non-invasively. We hypothesized that inflation of an anti-G garment was suitable to increase PCWP non-invasively in healthy elderly subjects. In 20 subjects, aged 70 +/- 4 years (mean +/- SD), before, immediately after, and 4 min after anti-G garment inflation to 52 mmHg, PCWP and mean pulmonary artery pressure (MPAP) were measured with a Swan-Ganz catheter, and mean arterial blood pressure (MAP) with Finapres, in supine and semi-recumbent position. Supine, PCWP (mmHg, mean +/- SD) increased from 9.9 +/- 2.1 to 15.5 +/- 3.9** immediately after inflation and 13.4 +/- 3.7** at 4 min; semi-recumbent from 8.9 +/- 2.0 to 17.5 +/- 3.3** and 14.7 +/- 2.9** (*P<0.05, **P< 0.001 versus before inflation). MPAP (mmHg) increased after inflation: supine 16.9 +/- 2.3 to 22.3 +/- 4.6** and 20.6 +/- 3.9** and semi-recumbent 15.7 +/- 2.8 to 24.3 +/- 5.1** and 22.5 +/- 3.5**, suggesting that increased preload was the primary effect of anti-G garment inflation. Supine MAP (mmHg) increased from 96.0 +/- 11.3 to 101.4 +/- 13.4** and 100.5 +/- 12.7* and semi-recumbent from 102.0 +/- 8.9 to 108.3 +/- 11.4** and 106.0 +/- 11.3*, suggesting an effect of increased afterload as well. The latter was supported by an increase in total peripheral resistance (d s cm(-5)) from 1346 +/- 299 to 1441 +/- 384 after 4 min (P = 0.057) and from 1461 +/- 341 to 1532 +/- 406 (P = 0.054), supine and semi-recumbent respectively, while cardiac output remained unchanged. Complications did not occur. We conclude that in healthy elderly subjects, anti-G garment inflation is a safe, non-invasive, method to induce a significant increase in PCWP. Our findings justify its application in future studies in which non-invasive temporary increase in PCWP is required.     

Ex vivo testing of the Quart arterial line filter

Arterial line filters are now routinely used in cardiac surgery in order to decrease the microemboli load to the patient. The Quart filter (Jostra, Hirrlingen, Germany) with a new planar construction design, an easy de-airing system and an integrated bypass, was tested for air filtration capacity and resistance to blood path in a standardized setting with surviving animals. Three calves (mean body weight: 71+/-3.4 kg) were connected to a standard cardiopulmonary bypass (CPB) circuit by jugular venous and carotid arterial cannulation with a mean flow rate of 3.5 l/min. The arterial line filter was challenged with upstream injections of boluses of air of 5, 10 and 15 ml, respectively. A Doppler ultrasound was positioned downstream on the arterial line to measure bubble count and size. The pressure drop through the filter was monitored at flow rates of between 1 and 6 l/min. At the end of the procedure the animals were weaned from the CPB and, thereafter, from the ventilator. After 7 days, the animals were sacrificed electively. This study shows that important quantities of air can be injected into the arterial line upstream of the filter with small volumes of small sized bubbles recorded downstream. With the 5 ml air bolus injection, mean values of 0.3+/-0.6 bubbles of 30 and 40 microm were detected, whereas with the 20 ml bolus, 32.6+/-8.7 bubbles of 10 microm, 3.7+/-1.1 bubbles of 30 microm, 3.3+/-0.6 bubbles of 40 microm and 0.7+/-1.1 bubbles of 50 microm were recorded. The blood path resistance at different blood flow rates was well within the acceptable range with a pressure drop of 20+/-0 and 26.6+/-5.7 mmHg at flow rates of 4 and 5 l/min, respectively. With its planar concept, the Quart filter offers good air filtering capacity both in terms of bubble count and size after injection of large boluses of air, without any increase of resistance to the blood path. Moreover, it offers a venting function and an integrated bypass system.     

Clinical application of the nitroglycerin lingual spray

The effect of sublingually administered nitrate spray was investigated with noninvasive methods. During 3 months, 82 patients were entered into the study: 40 with angina pectoris, 15 with acute myocardial infarction, 18 with hypertensive crisis, and 9 with left ventricular failure or acute pulmonary edema. The hemodynamic effects of two jets of nitroglycerin spray (0.8 mg Nitrolingual spray; Pohl-Boskamp, Hohenlocksted, Germany) was measured on heart rate, blood pressure, and flow velocity at baseline and 1, 5, and 10 minutes after drug administration. Flow velocities were measured through the left ventricular outflow tract and the mitral valve (early diastolic wave and atrial wave) with bedside Doppler echocardiography. The time to improvement and occurrence of adverse events was analyzed. Heart rate was constant after the therapy (75 +/- 8, 75 +/- 10, 75 +/- 10, and 75 +/- 9 beats per min; not significant), and systolic blood pressure decreased significantly 1 minute after administration and remained decreased throughout the examination (135 +/- 27, 124 +/- 21, 125 +/- 19, and 124 +/- 22 mm Hg, respectively; p < 0.001). The diastolic blood pressure was also significantly decreased (82 +/- 17, 79 +/- 14, 78 +/- 12, 78 +/- 14 mm Hg; p < 0.001). A significant increase in flow velocities in the left ventricular outflow tract was detected (90 +/- 8, 101 +/- 10, and 114 +/- 13 cm/s; p < 0.001) concomitantly with a significant increase in the early diastolic flow (46 +/- 4, 65 +/- 6, and 76 +/- 8 cm/s; p < 0.001) and the atrial wave (101 +/- 9, 110 +/- 10, and 118 +/- 9 cm/s; p < 0.001). This increase of flow velocity was less pronounced through the mitral valve than through the left ventricular outflow tract.